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GHY2
Hi Yield goljan pt2
| Question | Answer |
|---|---|
| Brain atrophy | ischemia; Alzheimer’s |
| Exocrine gland atrophy in CF | duct obstruction by thick secretions |
| Labile cells | stem cells (skin, marrow, GI tract) →←→⇦ |
| Stable cells | in G0 phase (smooth muscle, hepatocytes); can enter cell cycle (growth factors, hormones) |
| Permanent cells | cannot replicate; cardiac/striated muscle; neurons |
| Hypertrophy | increase in cell size (structural components, DNA) |
| LVH | increased preload (valve regurgitation), increased afterload (hypertension, aortic stenosis) |
| RVH | pulmonary hypertension |
| Bladder smooth muscle hypertrophy | prostate hyperplasia constricts urethra |
| Removal of kidney | hypertrophy of remaining kidney |
| Hyperplasia | increase in number of cells |
| Endometrial hyperplasia | unopposed estrogen (obesity, taking estrogen) |
| RBC hyperplasia | increased EPO (blood loss, ectopic secretion, high altitude) |
| Prostate hyperplasia | increased dihydrotestosterone (DHEA) |
| Gynecomastia | hyperplasia male breast tissue; normal in newborn, adolescent, elderly |
| Metaplasia | one adult cell type replaces another cell type |
| Squamous metaplasia in bronchus | smoking |
| Intestinal metaplasia in stomach | Paneth cells, goblet cells; H pylori chronic atrophic gastritis |
| Squamous metaplasia bladder | Schistosoma hematobium infection |
| Barrett’s esophagus | glandular metaplasia of distal esophagus; due to GERD |
| Dysplasia | atypical hyperplasia and metaplasia are precursors for cancer |
| Squamous dysplasia in cervix | human papilloma virus |
| Squamous dysplasia in bronchus | smoking |
| Necrosis | death of groups of cells |
| Coagulation necrosis | preservation of structural outline (due to ↑ lactic acid) |
| Infarction | pale (e |
| Liquefactive necrosis | brain infarct, bacterial infections; wet gangrene |
| Caseous necrosis | variant coagulation necrosis; granulomas due to TB/systemic fungi |
| Granulomas | activated macrophages (epithelioid cells); multinucleated giant cells; CD4 TH1 cells |
| Epithelioid cells | γ-interferon released by CD4 T cells activates macrophages |
| Multinucleated giant cells | fusion of epithelioid cells |
| Granulomas | type IV hypersensitivity |
| Enzymatic fat necrosis | associated with pancreatitis; soap formation (Ca2+ + fatty acids) |
| Fibrinoid necrosis | necrosis of immune reactions (immune vasculitis/endocarditis) |
| Postmortem necrosis | autolysis; no inflammatory reaction |
| Dystrophic calcification | calcification of damaged tissue; normal serum calcium |
| Dystrophic calcification | pancreatitis; atherosclerotic plaque |
| Metastatic calcification | calcification of normal tissue; increased serum calcium or phosphorus |
| Nephrocalcinosis | metastatic calcification of collecting tubule basement membranes |
| S/S nephrocalcinosis | polyuria due to nephrogenic diabetes insipidus; renal failure |
| Apoptosis | gene regulated individual cell death |
| Signals activating apoptosis | mullerian inhibitory factor, tumor necrosis factor, hormone withdrawal |
| Signal modulators of apoptosis | TP53 suppressor gene, BCL-2 genes |
| BCL-2 genes | anti-apoptosis gene; prevents cytochrome c from leaving mitochondria |
| Caspases | responsible for enzymatic cell death in apoptosis; proteases and endonucleases |
| Markers of apoptosis | eosinophilic cytoplasm, pyknotic (ink dot) nucleus |
| Apoptosis | loss Mullerian epithelium in male fetus; thymus involution; killing cancer cells |
| Histamine | key chemical in acute inflammation; mast cell; arteriole vasodilation; ↑ venular permeability |
| Rubor acute inflammation | redness; arteriole vasodilation (histamine) |
| Calor acute inflammation | heat; arteriole vasodilation (histamine) |